Co-Secretion of Aldosterone and Cortisol by an Adrenocortical Carcinoma

Kurtulmuş, Neslihan; Yarman, Sema; Azizlerli, H.; Kapran, Y

doi:10.1159/000079322

Cited by 11 publications

(8 citation statements)

References 18 publications

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“…This was believed to be the result of earlier symptoms due to hormonal excess and detection of smaller tumors [11]. Since then, several studies have contradicted this finding.…”

Section: Biochemical Functionmentioning

confidence: 99%

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Adrenocortical carcinoma

Roman

2006

Current Opinion in Oncology

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Pre-operative diagnostic advances in positron emission scanning are emerging as promising modalities for confirmation of malignancy of indeterminate adrenal masses. No significant advances in the treatment of adrenocortical carcinoma have been developed. Surgery remains the mainstay for primary and recurrent disease, including select patients with isolated liver metastases. Mitotane has remained the preferred adjuvant treatment agent, showing modest effect in patients with unresectable, residual or metastatic disease. Multi-institutional registries and trials need to be established, with multidisciplinary efforts focused on the development of new therapeutic strategies.

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“…This was believed to be the result of earlier symptoms due to hormonal excess and detection of smaller tumors [11]. Since then, several studies have contradicted this finding.…”

Section: Biochemical Functionmentioning

confidence: 99%

“…Only the malignant tumors had FDG uptake [22]. 11 C-metomidate (MTO) is a marker for 11 b-hydroxylase, and has been suggested as a novel PET tracer in adrenal imaging. Sixteen patients with adrenal masses underwent scanning with both MTO and FDG PET, followed by surgical resection and pathologic analysis.…”

Section: Diagnosismentioning

confidence: 99%

Adrenocortical carcinoma

Roman

2006

Current Opinion in Oncology

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“…We failed to rule out hypercortisolism definitely by a dexamethasone suppression test or an assessment of urinary cortisol concentration. However, since co- secretion of aldosterone and cortisol has previously been reported in adrenal tumours (Kurtulmus et al, 2004), a low-dose dexamethasone suppression test should be part of any endocrinological evaluation of an adrenal mass, also in those causing primary aldosteronism. The failure to diagnose subclinical autonomous glucocorticoid hypersecretion can endanger the patient who undergoes adrenalectomy because of possible postoperative development of secondary adrenal insufficiency.…”

Section: Discussionmentioning

confidence: 99%

Steroid Profile in an Adrenocortical Carcinoma Producing Aldosterone

Müssig¹,

Wehrmann²,

Horger³

et al. 2005

Exp Clin Endocrinol Diabetes

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We report a rare case of primary aldosteronism due to an adrenocortical carcinoma. A 61-year-old woman with a history of hypertension and hypokalemia was referred for evaluation of a 4.2 cm measuring adrenal mass without secondary signs of malignancy. Endocrinological testing was consistent with primary aldosteronism. The patient underwent surgical resection of the adrenal mass; histology revealed an adrenocortical carcinoma. Postoperatively blood pressure, serum potassium, and aldosterone returned to normal. Four months after adrenalectomy, the patient presented again with hypokalemic hypertension and was found to have metastatic disease. Endocrinological investigation revealed primary aldosteronism and subclinical autonomous glucocorticoid hypersecretion. Careful hormonal investigation should be obtained in patients with adrenal masses causing excessive aldosterone secretion. In uncertain cases of primary aldosteronism, we would suggest to measure 18-hydroxycortisol levels, as excessive amounts may indicate adrenocortical carcinoma.

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“…Adrenocortical carcinoma with production of both cortisol and aldosterone is even rarer. There have been a number of case reports of coproduction of aldosterone and cortisol in patients with adrenocortical carcinoma (158,180). Patients with carcinoma should be easily recognized as the adrenal tumor is often much larger than 3 cm, will have intermediate attenuation with CT imaging and often has a heterogeneous appearance.…”

Section: Anatomic Imagingmentioning

confidence: 99%

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Magill

2014

Comprehensive Physiology

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The renin-angiotensin-aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension. The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the actions of angiotensin II, chronic elevation in aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess aldosterone are heavily dependent on increased dietary salt intake as has been demonstrated in animal models and in humans. Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary aldosteronism has been found to occur in 5% to 13% of subjects with hypertension. In addition, patients with hyperaldosteronism have more end organ manifestations such as left ventricular hypertrophy and have significant cardiovascular complications including higher rates of heart failure and atrial fibrillation compared to similarly matched patients with essential hypertension. The pathophysiology, diagnosis, and treatment of primary aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper- and hypo-aldosteronism and unusual disorders of hypertension will also be reviewed in this article.

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Co-Secretion of Aldosterone and Cortisol by an Adrenocortical Carcinoma

Cited by 11 publications

References 18 publications

Adrenocortical carcinoma

Adrenocortical carcinoma

Steroid Profile in an Adrenocortical Carcinoma Producing Aldosterone

Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

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